S-nitrosylated GAPDH mediates neuronal apoptosis induced by amyotrophic lateral sclerosis-associated mutant SOD1(G93A)S-nitrosylated GAPDH mediates neuronal apoptosis induced by amyotrophic lateral sclerosis-associated mutant SOD1G93A
- Other Titles
- S-nitrosylated GAPDH mediates neuronal apoptosis induced by amyotrophic lateral sclerosis-associated mutant SOD1G93A
- Authors
- Lee, R.[Lee, R.]; Lim, J.M.[ Lim, J.M.]; Roh, K.-H.[ Roh, K.-H.]; Kim, J.H.[ Kim, J.H.]; Kang, S.[ Kang, S.]; Lee, J.E.[Lee, J.E.]; Choi, E.-J.[ Choi, E.-J.]
- Issue Date
- 2016
- Publisher
- TAYLOR & FRANCIS LTD
- Keywords
- Amyotrophic lateral sclerosis; deprenyl; GAPDH; S-nitrosylation; superoxide dismutase 1 (G93A)
- Citation
- ANIMAL CELLS AND SYSTEMS, v.20, no.6, pp.310 - 316
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- ANIMAL CELLS AND SYSTEMS
- Volume
- 20
- Number
- 6
- Start Page
- 310
- End Page
- 316
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/33856
- DOI
- 10.1080/19768354.2016.1259182
- ISSN
- 1976-8354
- Abstract
- Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with the selective loss of motor neurons in the brain, brain stem, and spinal cord. A number of the mutants of the human gene for superoxide dismutase 1 (SOD1) have been shown to cause familial ALS as a result of gain-offunction toxicity by an unknown mechanism. In this study, we show that glyceraldehyde-3phosphate dehydrogenase (GAPDH) functions as a critical mediator of the apoptotic cell death signaling cascade induced by the ALS-associated G93A mutant of human SOD1 [SOD1(G93A)]. We observed that SOD1(G93A) induces S-nitrosylation of GAPDH and the subsequent binding of GAPDH and Siah1 in NSC34 motor neuron-like cells. Furthermore, SOD1(G93A) promoted nuclear translocation of S-nitrosylated GAPDH in the cells. In addition, SOD1(G93A)-induced apoptotic cell death was inhibited by deprenyl, a chemical inhibitor of GAPDH S-nitrosylation, in NSC34 cells. Taken together, our findings suggest that S-nitrosylation of GAPDH plays a critical role in SOD1(G93A)-induced neuronal apoptosis.
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Collections - Samsung Advanced Institute for Health Sciences and Technology, SKKU > Samsung Advanced Institute for Health Sciences and Technology, SKKU > 1. Journal Articles
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